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本文引用的文献

1
Prenatal Air Pollution and Newborns' Predisposition to Accelerated Biological Aging.产前空气污染与新生儿加速生物衰老的易感性。
JAMA Pediatr. 2017 Dec 1;171(12):1160-1167. doi: 10.1001/jamapediatrics.2017.3024.
2
Telomere length dynamics in early life: the blood-and-muscle model.端粒长度在生命早期的动态变化:血液-肌肉模型。
FASEB J. 2018 Jan;32(1):529-534. doi: 10.1096/fj.201700630R. Epub 2017 Aug 29.
3
Genetic Variants Related to Longer Telomere Length are Associated with Increased Risk of Renal Cell Carcinoma.与端粒长度较长相关的遗传变异与肾细胞癌风险增加相关。
Eur Urol. 2017 Nov;72(5):747-754. doi: 10.1016/j.eururo.2017.07.015. Epub 2017 Aug 7.
4
Mutations, Cancer and the Telomere Length Paradox.突变、癌症与端粒长度悖论
Trends Cancer. 2017 Apr;3(4):253-258. doi: 10.1016/j.trecan.2017.02.005. Epub 2017 Mar 27.
5
Short Telomeres, but Not Telomere Attrition Rates, Are Associated With Carotid Atherosclerosis.端粒缩短而非端粒损耗率与颈动脉粥样硬化相关。
Hypertension. 2017 Aug;70(2):420-425. doi: 10.1161/HYPERTENSIONAHA.117.09354. Epub 2017 Jun 19.
6
Ancestry, Telomere Length, and Atherosclerosis Risk.血统、端粒长度与动脉粥样硬化风险。
Circ Cardiovasc Genet. 2017 Jun;10(3). doi: 10.1161/CIRCGENETICS.117.001718.
7
Exploring the Causal Pathway From Telomere Length to Coronary Heart Disease: A Network Mendelian Randomization Study.探索端粒长度与冠心病之间因果关系的途径:基于网络的孟德尔随机化研究。
Circ Res. 2017 Jul 21;121(3):214-219. doi: 10.1161/CIRCRESAHA.116.310517. Epub 2017 May 17.
8
Cellular Senescence: A Translational Perspective.细胞衰老:转化视角。
EBioMedicine. 2017 Jul;21:21-28. doi: 10.1016/j.ebiom.2017.04.013. Epub 2017 Apr 12.
9
Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging.衰老细胞的靶向凋亡可恢复组织稳态以应对化学毒性和衰老。
Cell. 2017 Mar 23;169(1):132-147.e16. doi: 10.1016/j.cell.2017.02.031.
10
Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study.端粒长度与癌症和非肿瘤性疾病风险的关联:一项孟德尔随机化研究。
JAMA Oncol. 2017 May 1;3(5):636-651. doi: 10.1001/jamaoncol.2016.5945.

端粒动力学与人类衰老相关疾病的思考。

Reflections on telomere dynamics and ageing-related diseases in humans.

机构信息

The Center of Human Development and Aging, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark, NJ 07103, USA

Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.

出版信息

Philos Trans R Soc Lond B Biol Sci. 2018 Mar 5;373(1741). doi: 10.1098/rstb.2016.0436.

DOI:10.1098/rstb.2016.0436
PMID:29335375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5784057/
Abstract

Epidemiological studies have principally relied on measurements of telomere length (TL) in leucocytes, which reflects TL in other somatic cells. Leucocyte TL (LTL) displays vast variation across individuals-a phenomenon already observed in newborns. It is highly heritable, longer in females than males and in individuals of African ancestry than European ancestry. LTL is also longer in offspring conceived by older men. The traditional view regards LTL as a passive biomarker of human ageing. However, new evidence suggests that a dynamic interplay between selective evolutionary forces and TL might result in trade-offs for specific health outcomes. From a biological perspective, an active role of TL in ageing-related human diseases could occur because short telomeres increase the risk of a category of diseases related to restricted cell proliferation and tissue degeneration, including cardiovascular disease, whereas long telomeres increase the risk of another category of diseases related to increased proliferative growth, including major cancers. To understand the role of telomere biology in ageing-related diseases, it is essential to expand telomere research to newborns and children and seek further insight into the underlying causes of the variation in TL due to ancestry and geographical location.This article is part of the theme issue 'Understanding diversity in telomere dynamics'.

摘要

流行病学研究主要依赖于白细胞端粒长度(TL)的测量,这反映了其他体细胞的 TL。白细胞端粒长度(LTL)在个体之间存在巨大差异——这一现象在新生儿中已经观察到。它具有高度的遗传性,女性比男性长,非洲血统的人比欧洲血统的人长。LTL 在由年龄较大的男性生育的后代中也更长。传统观点认为 LTL 是人类衰老的被动生物标志物。然而,新的证据表明,选择性进化力量和 TL 之间的动态相互作用可能会导致特定健康结果的权衡。从生物学的角度来看,TL 在与衰老相关的人类疾病中可能发挥积极作用,因为短端粒会增加与细胞增殖受限和组织退化相关的一类疾病的风险,包括心血管疾病,而长端粒会增加与增殖性生长增加相关的另一类疾病的风险,包括主要癌症。为了了解端粒生物学在与衰老相关的疾病中的作用,必须将端粒研究扩展到新生儿和儿童,并进一步深入了解由于祖籍和地理位置导致 TL 变化的根本原因。本文是主题为“理解端粒动力学多样性”的一部分。